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Mood disorders – review of structural MRI studies
- E. Serap Monkul, Gin S. Malhi, Jair C. Soares
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- Journal:
- Acta Neuropsychiatrica / Volume 15 / Issue 6 / December 2003
- Published online by Cambridge University Press:
- 24 June 2014, pp. 368-380
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- Article
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Background:
Mood disorders are related to considerable morbidity and mortality, and although there is little doubt that they are brain-based disorders, their neural correlates still remain elusive. A neuro-anatomic model of mood regulation comprising the prefrontal cortex, amygdala-hippocampus complex, thalamus, basal ganglia, and connections among these areas has been proposed.
Objective:We reviewed the evidence for regional brain abnormalities in bipolar disorder, and attempted to integrate available findings into a comprehensive pathophysiological model of illness.
Methods:A computerized Medline Ovid search was conducted for the period 1966–2002, and complemented by a manual search of bibliographical references from recent reviews. Articles meeting specified criteria were included.
Results:Hyperintense lesions in cortical and subcortical regions are the most consistently reported and widely studied structural abnormalities. Smaller prefrontal cortical volume is a common finding in bipolar disorder and unipolar depression. Enlarged amygdala (in bipolar disorder) and smaller hippocampus (in unipolar depression) have been reported by several groups. Decreased volumes (in unipolar depression) and increased or unaltered volumes (in bipolar disorder) of striatal structures have been reported.
Conclusions:Bipolar and unipolar mood disorders are associated with detectable structural brain abnormalities. The histopathology underlying such anatomical changes remains to be elucidated. To reach more definitive conclusions about neuroanatomical changes that take place during the course of mood disorders, prospective longitudinal studies are needed. Also, integration with functional imaging is necessary in order to elucidate the relevance of identified structural abnormalities.
Dissociable mechanisms for memory impairment in bipolar disorder and schizophrenia
- DAVID C. GLAHN, JENNIFER BARRETT, CARRIE E. BEARDEN, JIM MINTZ, MICHAEL F. GREEN, E. SERAP MONKUL, PABLO NAJT, JAIR C. SOARES, DAWN I. VELLIGAN
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- Journal:
- Psychological Medicine / Volume 36 / Issue 8 / August 2006
- Published online by Cambridge University Press:
- 31 May 2006, pp. 1085-1095
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Background. Although memory deficits are consistently reported in schizophrenia and bipolar disorder, the mechanisms underlying these impairments are poorly understood. Clarifying the nature and degree of overlap in memory deficits between the two illnesses could help to distinguish brain systems disrupted in these illnesses, and indicate cognitive remediation strategies to improve patient outcomes.
Method. We examined performance on a non-verbal memory task in clinically stable out-patients with bipolar disorder (n=40), schizophrenia (n=40), and healthy comparison subjects (n=40). This task includes conditions in which distinct mnemonic strategies – namely, using context to organize familiar stimuli or using holistic representation of novel stimuli – facilitate performance.
Result. When compared to a reference condition, bipolar patients had deficits consistent with organizational dysfunction and poor detection of novel information. Although patients with schizophrenia performed worse than the other groups, they were only differentially impaired when organizational demands were significant. Task performance was not correlated with severity of clinical symptomatology.
Conclusions. This pattern of distinct memory impairments implies disturbances in partially overlapping neural systems in bipolar disorder and schizophrenia. Evidence of impairment in detection of novel stimuli that is unique to bipolar disorder suggests that, while the absolute level of cognitive dysfunction is less severe in bipolar disorder as compared to schizophrenia, subtle disruptions in memory are present. These findings can be used to plan targeted cognitive remediation programs by helping patients to capitalize on intact functions and to learn new strategies that they do not employ without training.